This project is directed to study of interrelationships between disturbances of systemic and intrarenal hemodynamics and the alterations of kidney function and sodium excretion which occur in cardiovascular diseases such as hypertension and congestive heart failure. The present investigations propose to explore the general hypothesis that renal vasuclar tone during alterations in sodium balance, edema formation and in certain subsets of patients with hypertensive disease and/or oliguric renal failure results from the balanced interplay of vasoconstrictor (renin-AII, catecholamines) anfd vasodilator (prostaglandins, kallikrein-kinin) intrarenal hormones. Experiments are designed to correlate the changes in systemic hemodynamics, intrarenal blood flow (microshperes) and tubular sodium reabsorption which occur during sodium depletion and edema formation in animal models with the arterial and renal venous concentrations and the urinary excretion rates of the vasoconstrictor and vasodilator hormones. Additional studies are proposed to investigate the extent to which arterial blood pressure, renal vascular resistance and the blood pressure response to increased sodium intake are modulated by adrenergic neurotransmitter, renin-AII, urinary kallikrein and the renal prostaglandins.